Abnormal hepatic lipid metabolism is a major contributor to non-alcoholic fatty liver disease (NAFLD). NAFLD is strongly associated with the development of insulin resistance and type 2 diabetes.

SerpinA3N (serine (or cysteine) peptidase inhibitor clade A member 3N) is a member of the serpin family of proteins, a group of proteins that inhibit serine proteases. It has been shown to play a role in glucocorticoid-induced myopathy, and is upregulated by a high fat diet.

In this paper, Tran et al. identify the role of serpinA3N in governing NAFLD progression and glucose homeostasis. They characterise a serpinA3N hepatic knockout, detailing protected glucose tolerance and insulin sensitivity. This model also demonstrates resistance to diet-induced obesity. The study shows, for the first time, that co-ordination of leptin and insulin may, in part, be driven by serpinA3N, and that this protein may have an important role in the manifestation of NAFLD.

Read the full article in Journal of Endocrinology 256 e220073